The purpose of this project is to investigate the biological basis of very early visual information processing dysfunction in patients with schizophrenia. Early auditory and visual information processing deficits are often considered to be core cognitive deficits in schizophrenia. The proposed studies will be done using a "backward masking" paradigm, which is unique in its ability to measure pre-attentive visual information processing. Patients with schizophrenia consistently take longer to process information on this task. This finding is thought to reflect slower transfer of information from iconic, or pre-attentive, processing to short term memory, where it enters conscious awareness. Such a deficit in the initial stages of information processing could lead to faulty intake of information and may ultimately result in some of the clinical symptomatology of these patients. In order to elucidate the neural basis of backward masking dysfunction, the proposed project will determine whether the backward masking deficit: 1) is present during both drug-free andantipsychotic medication periods in patients with schizophrenia; and 2) is due to increased transient cell activity in the visual system of patients with schizophrenia. The proposed studies will enable us to begin to elucidate the biological basis of what is thought to be a fundamental deficit in schizophrenia - a deficit in the earliest stages of information processing. These studies will lay the groundwork for future studies addressing the level of the visual processing deficit, examining dopamine and GABA function in backward masking, and determining whether backward masking and aberrant transient cell activity are genetic vulnerability markers of schizophrenia spectrum disorders. These studies have the potential to elucidate the anatomical, pharmacological, and genetic basis of what may be a core cognitive deficit in schizophrenia - a deficit in early information processing.